Key result
Active orthostatism in T2D patients with autonomic neuropathy and postural hypotension showed impaired noradrenaline response at 20 min (+656±295 pmol/L, p=NS) but preserved renin-angiotensin response.
Why the study?
Does active orthostatism alter neurohormonal responses in type 2 diabetic patients with autonomic neuropathy and postural hypotension compared to controls?
Population
40 subjects including 10 healthy controls, 9 type 2 diabetes patients without autonomic neuropathy, 14 T2D…
Comparison
Active orthostatism for 2, 5, and 20 minutes vs Supine position (baseline) and healthy controls
Design
Cross-sectional
Follow-up
20 minutes
Authors
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Preserved RAAS response despite impaired noradrenaline supports compensatory mechanisms in T2D orthostatic hypotension; leaves open targeted interventions.
Observational (n=40)
Does active orthostatism alter neurohormonal responses in type 2 diabetic patients with autonomic neuropathy and postural hypotension compared to controls?
In type 2 diabetic patients with autonomic neuropathy and postural hypotension, the renin-angiotensin-aldosterone system response to orthostatism is preserved despite impaired catecholamine responses.
Jarmuzewska et al. (2003) conducted an observational in Type 2 diabetes with autonomic neuropathy and postural hypotension (n=40). Active orthostatism vs. Supine position (baseline) was evaluated on Neurohormonal responses (plasma noradrenaline, adrenaline, plasma renin activity, and aldosterone). Active orthostatism in T2D patients with autonomic neuropathy and postural hypotension showed impaired noradrenaline response at 20 min (+656±295 pmol/L, p=NS) but preserved renin-angiotensin response.
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